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PubMed2003

Surgical management of amiodarone-induced thyrotoxicosis.

OBJECTIVE: Amiodarone can cause thyroid dysfunction in patients with or without previous thyroid disease. With increased use from its placement in advanced cardiac life support guidelines and cardiac transplant programs, the incidence of amiodarone-induced thyrotoxicosis (AIT) will likely increase. Medical management is complex and nonuniform and frequently fails. This study investigates the role of surgery in AIT and proposes indications for surgical management. STUDY DESIGN AND SETTING: Two AIT case reports at a tertiary care institution and 31 surgical AIT cases in the world literature are reviewed. METHODS: The 2 AIT cases involved patients with cardiomyopathy and resistant arrhythmias. Despite medical therapy, both patients' conditions failed to improve. Thirty-one surgical cases of AIT in the literature are evaluated with respect to symptoms and onset, medical therapy, AIT classification, pathology, perioperative management, and complications. RESULTS: Both patients underwent total thyroidectomy without difficulty or complication, one as an overnight stay and one as an inpatient with an intraaortic balloon pump. One patient received a successful cardiac transplant and the other remains a viable candidate. In the literature, the majority (80%) of surgical cases are AIT type II (less common type) with no underlying thyroid disease. Range and duration of symptoms varied, in addition to type and duration of medical management. Almost all patients underwent total thyroidectomy, and all were successful with no mortality and minimal morbidity. CONCLUSION: AIT can develop in any patient during or after amiodarone therapy. Medical management is extremely difficult due to the absence of a proven therapeutic armamentarium, and surgery offers a safe, viable option. Surgical management should play a larger role in treatment algorithms and should be strongly considered for patients whose conditions necessitate continuation of amiodarone, or with severe symptoms resistant to medical therapy.

Adult↗
PubMed1999

[Is there a need for treatment in subclinical hypo- and hyperthyroidism?].

Subclinical thyroid dysfunction is characterized by normal levels of thyroid hormones but abnormal values of thyrotropin (TSH) in an asymptomatic individual. Subclinical hypothyroidism is a common disorder with a prevalence of about 7 to 8% in women (most frequently in females over 50 years), and about 3% in men. It is characterized by elevated serum TSH in the presence of normal concentrations of serum thyroxine. Patients with TSH levels about 12 mU/L (and with positive antithyroidal antibodies) have the highest risk for developing overt hypothyroidism. Therefore, these patients will require L-thyroxine treatment. In patients with TSH < 12 mU/L, the indication for therapy depends on the etiology, on risk factors and concomitant diseases (e.g. strumectomy, coronary heart disease, depression, infertility). Subclinical hyperthyroidism (TSH suppression syndrome) is characterized by normal thyroid hormone concentrations but diminished serum TSH. Most frequently, this disorder is caused by exogenous L-thyroxine treatment. The endogenous form of subclinical hyperthyroidism mainly caused by nodular goiter has a prevalence of up to 20% in patients with large goiters. In patients with subclinical hyperthyroidism, there is an increased risk for development of atrial fibrillation and for a decrease in bone mass in postmenopausal women. In the majority of patients measurable TSH levels can be detected before or after stimulation with TRH. This formally excludes overt hyperthyroidism in such patients. Frequently, there is no need for treatment but follow-up is important. However, in patients with subclinical hyperthyroidism associated with atrial fibrillation a therapy with antithyroid drugs, beta-blockers or radioiodine must be considered.

Diagnosis, Differential↗
PubMedDate not supplied

Amiodarone-induced thyrotoxicosis: a case for surgical management.

OBJECTIVE: Amiodarone can cause the development of thyroid dysfunction in patients with or without previous thyroid disease. Although most cases of amiodarone-induced thyrotoxicosis (AIT) are mild, a significant number become life threatening. Because of its pharmacokinetics, simply discontinuing amiodarone provides no relief and can worsen the patient's condition. Medical management frequently fails, and many patients cannot discontinue amiodarone because of its effect against resistant arrhythmias. METHODS: This retrospective chart review of a case at a tertiary care institution presents the case of a fifty-five-year-old male with dilated cardiomyopathy and no previous thyroid disease. The patient was in normal sinus rhythm on amiodarone for control of atrial fibrillation. He experienced the acute onset of symptoms with return to atrial fibrillation resistant to cardioversion. Physical examination, laboratory tests, and imaging findings were all consistent with a diagnosis of AIT. An attempt to withdraw amiodarone resulted in severe ventricular tachyarrhythmias. RESULTS: Despite medical treatment, the patient's condition continued to deteriorate. Because amiodarone was the only effective drug, surgical treatment was elected. The patient underwent a total thyroidectomy and experienced no difficulties or complications. Postoperatively, the patient's condition improved, and he was successfully cardioverted. CONCLUSIONS: Although an uncommon clinical entity, life-threatening AIT has been reported. Thyrotoxicosis can develop in any patient during or after amiodarone therapy. Medical management of this entity is extremely difficult because of the lack of a proven, consistent therapeutic armamentarium. Surgical management should be considered for patients whose conditions necessitate the continuation of amiodarone or those with severe symptoms resistant to medical therapy.

Amiodarone↗
PubMed2006

Status of anti-thyroid peroxidase during normal pregnancy and in patients with hyperemesis gravidarum.

Autoimmune thyroid diseases (AITD) comprising Hashimoto's thyroiditis, primary myxedema, and Graves' disease are associated with autoantibodies directed against thyroglobulin and thyroid peroxidase (anti-TPO). Anti-TPO occur in 10% of pregnant women, half of whom reportedly develop postpartum thyroid dysfunction. We recently published data on the thyroid function reference ranges in pregnant Chinese but the AITD status of our cohort was unknown. In view of this missing information we have measured anti-TPO in specimens from our cohort stored at -80 degrees C, and compared these to those of patients with hyperemesis gravidarum (HG) and nonpregnant controls. After eliminating 3 outliers from 47 nonpregnant controls, the anti-TPO concentration range was 2.2-14.7 kIU/L (n = 44). In 282 pregnant control subjects, the anti-TPO levels were less than 14.7 kIU/L (upper limit of nonpregnant controls) in 189 (67%); between 14.7-55 kIU/L in 82 (29.1%); and greater than 55 kIU/L in 11 (3.9%). The percentage of women with anti-TPO greater than 14.7 kIU/L during the first, second, and third trimesters were 47% (30/64), 39% (49/126), and 16% (15/92), respectively. Anti-TPO level was significantly higher in pregnant controls compared to nonpregnant controls and patients with HG. With reference to other studies in which anti-TPO levels greater than 60 kIU/L were considered pathologic, we conclude that more than 96% of our pregnant controls were without AITD and the data on thyroid function reference ranges we previously reported remain valid.

Adult↗
PubMed1998

Diagnosis and management of congenital hypothyroidism.

Thyroid hormones are integral to the development and maturation of the central nervous system as well as normal growth and development. Comprehensive knowledge of the maturation and function of the thyroid gland is essential to understanding the pathophysiology of thyroid dysfunction. Early diagnosis and appropriate treatment in thyroid disease are imperative for normalization of thyroid hormone ratios. Optimal management includes early introduction and strict adherence to a regimen of L-thyroxine and routine monitoring of thyroid levels throughout life. Parents need to understand the importance of consistent medication administration and daily assessment of well-being because these actions are crucial to the attainment of an optimal level of development for infants with congenital hypothyroidism.

Congenital Hypothyroidism↗
PubMed1990

Thyroid adenoma following treatment of acute lymphocytic leukemia.

Sequelae of the treatment of children with acute lymphocytic leukemia (ALL) include multiple effects on the endocrine system, especially as it relates to growth and puberty. Thyroid dysfunction, and in particular, the occurrence of thyroid neoplasia, has been only rarely described. We report the development of benign thyroid neoplasms in two patients 9 years following the diagnosis and treatment of ALL. Both patients were clinically and biochemically euthyroid with noncystic "cold" nodules found on thyroid scan. In light of these observations, and along with previous reports of malignant thyroid neoplasia in children with ALL, long-term careful observation of children successfully treated for ALL is indicated.

Adenoma↗
PubMed1989

Thyrotropin and prolactin responses to thyrotropin-releasing hormone in premenstrual syndrome.

Recent reports of altered TSH responsiveness to its releasing hormone (TRH) in women with premenstrual syndrome (PMS) suggested that subclinical hypothyroidism may be responsible for the mood changes, such as depression, that occur in these women. In this study we measured basal and TRH-stimulated serum TSH and PRL levels in 15 women with PMS and in 19 age-matched normal women. The mean baseline serum TSH concentrations were similar in the 2 groups in both the follicular [normal, 1.3 +/- 0.2 (+/- SE); PMS, 0.9 +/- 0.2 mU/L] and luteal (normal, 1.1 +/- 0.2; PMS, 1.1 +/- 0.2 mU/L) phases of the cycle. The mean baseline serum PRL levels also were similar in the 2 groups in the follicular (normal, 16 +/- 2; PMS, 13 +/- 2 micrograms/L) and luteal (normal, 13 +/- 2; PMS, 14 +/- 2 micrograms/L) phases of the cycle. After TRH administration, peak serum PRL and TSH levels were reached at 15 and 30 min, respectively, and the response curves were virtually identical in the 2 groups in both phases of the cycle. One normal woman had elevated basal and TRH-stimulated TSH concentrations compatible with subclinical hypothyroidism, but had normal noncyclic scores on her prospective rating scales. Our findings suggest that PMS is not associated with thyroid dysfunction or abnormal PRL secretion and that thyroid hormone replacement therapy is not indicated in this condition.

Adult↗
PubMed1999

Clinical characteristics of amiodarone-induced thyrotoxicosis and hypothyroidism in Japan.

Since amiodarone was introduced in Japan in 1992, the incidence of the drug-induced thyroid dysfunction has been increasing. We studied the thyroid function of 13 patients with amiodarone-induced thyrotoxicosis (AIT) and 11 patients with amiodarone-associated hypothyroidism (AAH) who had been referred to our Institute in the last 6 years. AIT and AAH developed after 39+/-21 and 20+/-16 months of amiodarone treatment, respectively. One patient developed AAH followed by AIT. The AIT ranged from subclinical to overt thyrotoxicosis. Four patients with moderate to marked AIT were treated with methimazole. Their thyrotoxicosis persisted for 3 to 9 months, despite administration of antithyroid agents. One patient with mild thyrotoxicosis was treated with prednisolone, resulting in a euthyroid state in a few months. Eight patients with asymptomatic to moderate thyrotoxicosis resolved spontaneously without any treatment. In four asymptomatic patients with AIT, serum levels of T3 and T4 were in the upper normal range or slightly high (< 12 microg/dl), accompanied by suppressed TSH (<0.1 microU/ml) and high thyroglobulin levels, suggesting destruction-induced thyrotoxicosis. Such a subclinical thyrotoxicosis developed repeatedly in one patient. Ultrasonographic studies revealed no nodular lesion in the thyroid, and color flow Doppler sonography demonstrated no hypervascularity in the thyroid gland in any AIT patient. Although it is postulated in Europe that there are two types of AIT, namely type I, which develops in patients with latent Graves' disease or toxic multinodular goiter, and type II, which develops in an apparently normal thyroid as destructive thyroiditis, all AIT patients we have seen so far had developed destructive type AIT. Sufficient intake of iodide and a very low incidence of toxic multinodular goiter may account for the rare incidence of type I AIT in our country. Mild to moderate AIT resolved spontaneously without discontinuing amiodarone, but it was discontinued in two of 13 AIT patients because of extrathyroidal adverse reactions.

Adult↗
PubMed1997

Effects of amiodarone on thyroid function.

PURPOSE: To review the literature on the effects of amiodarone on thyroid physiology and management of amiodarone-induced thyroid disease. DATA SOURCES: English-language articles identified through a MEDLINE search (for 1975 to 1995, using the terms amiodarone and thyroid) and selected cross-referenced articles. STUDY SELECTION: Articles on the effects of amiodarone on thyroid physiology and function tests and occurrence, recognition, and management of amiodarone-induced thyroid disease. DATA EXTRACTION: Data were manually extracted from selected studies and reports; emphasis was placed on information relevant to the practicing clinician. DATA SYNTHESIS: Amiodarone can have many effects on thyroid function test results, even in the absence of hyperthyroidism or hypothyroidism. It may cause an increase in serum levels of thyroxine, reverse triiodothyronine, and thyroid-stimulating hormone and a decrease in serum triiodothyronine levels. Thyrotoxicosis occurs in some patients and is related to several pathogenetic mechanisms. It often present dramatically with obvious clinical manifestations and further changes in thyroid function test results. Medical options include therapy with thionamides, perchlorate, and prednisone. Radioactive iodine is of little use. Thyroidectomy is effective and is the only measure that consistently allows continued use of amiodarone. Unlike thyrotoxicosis, hypothyroidism is related to a persistent Wolff-Chaikoff effect and often has a vague presentation. The goal of treatment of amiodarone-induced hypothyroidism is to bring serum thyroxine levels to the upper end of the normal range, as often seen in euthyroid patients who are receiving amiodarone. CONCLUSIONS: Thyroid dysfunction commonly occurs with amiodarone therapy. It may be difficult to recognize the dysfunction because of the many changes in thyroid function test results that occur in euthyroid patients who are receiving amiodarone. Effective strategies exist for the management of hyperthyroidism and hypothyroidism; these should be tailored to the needs of the individual patient.

Amiodarone↗
PubMed1994

Clinical use of laboratory thyroid tests and investigations.

Laboratory thyroid testing involves in vitro tests for autoimmune thyroid disease, thyroid dysfunction and neoplasia, in vivo investigations of thyroid function, and investigations of thyroid morphology. The authors describe, in tabular form, the diagnostic information carried by the tests and their clinical utility as well as clinically relevant interferences.

Adult↗
PubMed1996

Visual Evoked Potential (VEP)--dependable marker for CNS affection in thyroid diseases.

The mean latency and amplitude of P100 component of VEP were studied in forty three controls and eighty nine cases of thyroid dysfunction [Hypothyroid-28; Hyperthyroid-32 and probable Thyroiditis-29 (inclusive of 21 cytology proved)]. The mean latency in hypothyroid, hyperthyroid and probable thyroiditis subjects were 110.69, 111.41 and 109 m.sec in comparison to 101.91, 102.0 and 101.08 m. sec. respectively in controls (p < 0.005). The mean amplitude being 1.34, 6.34 and 2.41 microvolts in hypothyroid, hyperthyroid and probable thyroiditis subjects in comparison to 4.79, 4.16 and 4.59 microvolts respectively in controls (p < 0.005).

Adult↗
PubMed2001

[Pregnancy in women with thyroid cancer treated with suppressive doses of L-thyroxine].

UNLABELLED: The aim of the study was to estimate the dose of thyroxine required by pregnant women who had undergone total thyreoidectomy and radioiodine treatment for thyroid cancer. Material consisted of 4 pregnant women, aged mean 30.8 years. One of patients was studied during 2 consecutive pregnancies. The daily mean dose of thyroxine was 175 micrograms. The control group consisted of 7 women with primary hypothyroidism aged mean 33.5 years, who were treated with replacement doses of thyroxine. One of them was pregnant twice. The mean daily dose of thyroxine was 106.3 micrograms. The estimation of TSH, fT4 were repeated every 4 weeks. RESULTS: In all cases natural deliveries took place. All infants were alive and had no congenital malformations and no clinical or biochemical thyroid dysfunction was found. Pregnant women treated for thyroid cancer needed to have optimized their suppressive therapy by increasing the dose of thyroxine by 26% at the first trimester, 27% at the second and 38% at the last one. Statistically significant increase was found at the 1st trimester of pregnancy and it remained at the same level till the delivery. Pregnant hypothyroid women needed to have optimized their replacement thyroxine therapy by increasing of the dose by 53% at the first trimester, by 49% at the second and by 53% at the last one. Similarly to the 1st group of patients, we noticed statistically significant increase at the 1st trimester of pregnancy. CONCLUSION: In pregnant women who have been previously treated for thyroid cancer the suppressive dose of thyroxine needs to be increased by 26-38% which is slightly less than the increase of the replacement dose in hypothyroid pregnant women.

Adult↗
PubMedDate not supplied

[Serum antithyroid antibodies in patients with pernicious anemia].

We investigated the incidence of thyroid auto-antibodies and their relationship to antigastric antibodies in 20 euthyroid patients with pernicious anaemia. To evaluate possible thyroid dysfunction we also measured total level of thyroid hormones (TT3 and TT4) and TSH in our patients. Histologic evidence of autoimmune atrophic gastritis and intestinal metaplasia was obtained in 15 patients. We found that it was surprisingly high incidence of thyroid auto-antibodies in patients with pernicious anaemia, particularly in the group with intestinal metaplasia (antithyreoglobulin antibodies 71% and antimicrosomal antibodies 100%). The incidence of antigastric antibodies in these patients was similar to that of those with significant antithyroid antibodies (16/18). Total triiodo thyronine and TSH were significantly higher in the patients with pernicious anaemia than in the control group (p less than 0.05), in the normal range. The results of our study suggest that this upset in immunological physiology is due to a more generalized defect in immune tolerance.

Aged↗
PubMed1993

Thyroid autoimmunity and female gender.

Sexual dimorphism exists in regard to the immune response between women and men, and it accounts for the greater prevalence of thyroid autoimmunity in women. Similarly to the human situation a sex-related susceptibility to autoimmune thyroiditis is evident in animal models. A direct influence of genes on sex chromosomes (X or Y) on the immune response has been postulated in some models of autoimmune thyroiditis in rats. On the other hand sex hormones have been implicated to explain the majority of sex differences in the autoimmune response against the thyroid. A state of immune suppression during pregnancy influences the clinical course of autoimmune thyroid diseases, in that a typical amelioration during pregnancy is accompanied by aggravation following delivery. This immunologic rebound phenomenon may also underly the post partum thyroid dysfunction in otherwise healthy women with a genetic predisposition to autoimmune thyroid disease. Thyroid autoimmunity also interferes with the female reproductive function. Hypothyroidism and less frequently hyperthyroidism due to thyroid autoimmune disorders may produce menstrual dysfunction, anovulation and eventually infertility. Maternal hyper- or hypothyroidism can affect the outcome of pregnancy, producing a higher incidence of miscarriages, maternal complications, and congenital malformations. Untreated maternal hypothyroidism produced by Hashimoto's disease during pregnancy can impair the neurological development of the fetus due to a reduced availability of maternal thyroxine during early gestation.2+ More specifically, fetal and/or neonatal hypo- or hyperthyroidism produced by the transplacental passage of maternal thyroid autoantibodies can impair growth and neuropsychological development of affected children.

Female↗
PubMed1998

Occurrence of thyroid autoimmunity and dysfunction throughout a nine-month follow-up in patients undergoing interferon-beta therapy for multiple sclerosis.

Thyroid autoimmunity and dysfunction are a well known side effect of IFN alpha therapy for viral hepatitis and tumors, while the IFN beta effects on the thyroid gland in neurological patients have not been studied. The aim of this longitudinal study was to look for the appearance of thyroid autoimmunity as well as for the occurrence of overt thyroid disease in the patients affected by multiple sclerosis (MS) treated with IFN beta 1b. Eight patients (4 males, 4 females) undergoing r-IFN beta 1b treatment (8 M.U. every other day for 9 months) for relapsing remitting multiple sclerosis entered the study. We have analyzed thyroid function parameters and auto antibody levels before and after 1, 2, 3, 6 and 9 months of therapy. None of them referred to familiar thyroid pathology or presented clinically overt thyroid disease except for one patient (case 4) who showed TPO-Ab pretreatment positivity and another (case 8) who was in therapy with Levothyroxine 100 microg/die for multinodular goiter. The number of patients with appearance of thyroid antibodies has slowly increased, until the third month of therapy with 3 patients out of 7 positive for TPO-Ab. The only case of overt thyroid dysfunction reported by us appeared after nine months of therapy and consisted of a hypothyroidism. Our data suggest that short-term interferon beta treatment is able to induce thyroid autoimmunity (42.8%) and dysfunction (12.5%).

Adult↗
PubMed2004

Subclinical thyroid disease: clinical applications.

Subclinical hypothyroidism and hyperthyroidism are diagnoses based on laboratory evaluation with few if any clinical signs or symptoms. Subclinical hypothyroidism is defined as an elevation in serum thyroid-stimulating hormone (TSH) above the upper limit of the reference range (0.45-4.5 mIU/L) with normal serum FT4 concentration; subclinical hyperthyroidism is defined as a decrease in serum TSH below the reference range with normal serum FT4 and T3 concentrations. Though these conditions represent the earliest stages of thyroid dysfunction, the benefits of detecting and treating subclinical thyroid disease are not well established. Most persons found to have subclinical thyroid disease will have TSH values between 0.1 and 0.45 mIU/L or between 4.5 and 10 mIU/L, for which the benefits of treatment are not clearly established; treatment may be beneficial in individuals with serum TSH lower than 0.1 mIU/L or higher than 10 mIU/L. This article illustrates approaches to managing patients with subclinical hypothyroidism and hyperthyroidism through 5 case scenarios that apply the principles of evidence-based medicine. Because of the substantial uncertainty concerning the consequences of untreated subclinical hypothyroidism and hyperthyroidism, as well as the benefit of initiating treatment, patient preferences are important in deciding on management of subclinical disease.

Adult↗
PubMed1995

Low-dose IL-2 treatment: activation of discrete T- and NK-cell sub-populations in vivo.

The activation of T- and NK-cell sub-populations in vivo was evaluated in a phase-I study (18 patients) with a 3-month course of low-dose s.c. IL-2, 1, 3 and 6 x 10(6) IU/day once daily, 6 days a week. At the higher doses, we observed early on (day 15) an increase in CD3+ CD56-, CD3- CD56+ and CD56+ DR+ cell counts, as well as an increase in circulating sIL-2R and non-MHC-restricted cytotoxicity against K562 and Daudi cells. In contrast, at the lowest dose, T- and NK-cell counts were not appreciably altered, while a substantial increase in NK cytotoxic activity was still observed. In addition, thyroid dysfunction resembling that described in auto-immune thyroiditis, was documented in 6 out of the 14 patients studied. Using a high-resolution method analyzing CDR3 sizes of TCR beta transcripts, we observed the appearance of dominant T-cell clonotypes in 1 patient out of 2 analyzed, corresponding to the clonal expansion of T cells primed in vivo. Overall, these results show that long courses of low-dose s.c. IL-2 treatment lead to the activation of discrete T- and NK-cell sub-populations.

Carcinoma, Renal Cell↗
PubMed1990

Prevalence of thyroid abnormalities in patients with dermatitis herpetiformis and in control subjects with HLA-B8/-DR3.

PURPOSE: The prevalence of thyroid dysfunction as measured by the presence of overt thyroid disease, abnormal results of thyroid function tests, or antithyroid antibodies was compared in patients with dermatitis herpetiformis (DH) and a normal control group who had the HLA-B8/-DR3 haplotype. PATIENTS AND METHODS: The study population consisted of 56 patients with DH and 26 control subjects with the HLA-B8/-DR3 haplotype. All were examined for thyroid function abnormalities and thyroid autoantibodies. RESULTS: Patients with DH had a statistically significant increase in the prevalence of abnormal thyroid function test results and autoantibodies: 32% versus 4% for controls (Z = 2.01, p less than 0.02). In patients with DH, hypothyroidism was the most common thyroid abnormality (12 of 56) followed by hyperthyroidism (four of 56). Two patients had normal thyroid function test results with thyroid autoantibodies. Risk factors for thyroid abnormalities in patients with DH were increasing age (chi 2 = 6.55, p less than 0.02, significant) and the presence of thyroid microsomal antibodies. The HLA-B8/-DR3 haplotype was not a risk factor for thyroid abnormalities. CONCLUSION: The findings suggest that thyroid disease is independently associated with DH. Examination of patients with DH should include thyroid function tests along with assays for antithyroid antibodies.

Adult↗